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Biomedical subjects

D G Ward

Publications and source records attributed to D G Ward.

At least 37 records · Page 2Linked to original sources
PubMed1987

A blood pressure lowering effect of lesions of the caudal periaqueductal gray: relationship to basal pressure.

Basal mean arterial pressure (MAP) measured one week following placement of pontine lesions was markedly lower (-27.85 mm Hg) in cats with bilateral lesions of the caudal periaqueductal gray than in cats with bilateral lesions of the area anteroventral to the locus coeruleus. Regression models of the relationship between basal arterial pressure (MAPbasal) and the change in arterial pressure (MAPchange) after the lesions indicate that lesions of the caudal periaqueductal gray led to a marked decrease in MAP in animals with an elevated basal MAP (MAPchange = MAPbasal x (-1.182) + 139.433; r = -0.902; P less than 0.002). In contrast, lesions of the area anteroventral to the locus coeruleus had no such effect (MAPchange = MAPbasal x (-0.363) + 56.49; r = -0.375; P greater than 0.1). The region of the caudal periaqueductal gray affecting MAP appears anterior to the locus coeruleus and through intrinsic neurons or fibers of passage may play a critical role in control of arterial pressure.

Animals↗
PubMed1987

Lesions of the caudal periaqueductal gray prevent compensation of arterial pressure during hemorrhage.

Arterial pressure normally changes very little during small hemorrhage. In cats with bilateral lesions of the region of the caudal periaqueductal gray arterial pressure and renal vascular resistance decreased rapidly and precipitously during a 10 ml/kg X 3 min-1 hemorrhage. This lack of compensation was pronounced in response to a hemorrhage one week after lesioning but was not seen 1 h after lesioning in separate experiments. The critical region appears anterior and dorsal to the locus coeruleus and medial to the parabrachial nuclei.

Animals↗
PubMed1985

Rostral pontine and caudal mesencephalic control of arterial pressure and iliac, celiac and renal vascular resistance. I. Anatomic regions.

The rostral pons and caudal mesencephalon in 26 cats were electrically stimulated (greater than 2400 sites) while measuring arterial pressure and iliac, celiac and renal vascular resistance. Areas active in control of arterial pressure and iliac vasoconstriction were located in the marginal nucleus of the brachium conjunctivum (BCM) and in parts of the central tegmental fields (FTC) of the mesencephalon. Areas active in control of celiac and renal vasoconstriction were confined to the BCM. Areas active in control of iliac and celiac vasodilation were generally found ventral to the constrictor areas in the FTC of the mesencephalon. Stimulation of the caudal periaqueductal grey, locus caeruleus and underlying reticular formation elicited no change in any parameter measured. These findings suggest that multiple pathways for control of arterial pressure and vasoconstriction pass through or synapse in a discrete region of the dorsal rostral pons that is limited to the BCM.

Adrenocorticotropic Hormone↗
PubMed1985

Rostral pontine and caudal mesencephalic control of arterial pressure and iliac, celiac and renal vascular resistance. II. Separate control and topographic organization.

A dense mapping of the rostral pons and caudal mesencephalon was performed in 26 cats using electrical stimulation while measuring arterial pressure and iliac, celiac and renal vascular resistance to determine if these vascular beds are controlled separately. It was found that the central tegmental fields (CTF) of the mesencephalon contained a large area active in control of iliac vascular resistance and a smaller area active in control of renal vascular resistance. It was found that the marginal nucleus of the brachium conjunctivum (BCM) contained areas active in control of all three vascular beds studied. To determine if the BCM controlled regional vascular beds differently, the relationship between changes in vascular resistance in each bed and changes in arterial pressure were examined quantitiatively using regression analysis and the slopes of the regression lines were shown to be different (P less than 0.001). Further analysis of the relationships of changes in vascular resistance of pairs of vascular beds indicated that vascular beds are controlled differently in response to electrical stimulation of the BCM.

Animals↗
PubMed1984

Electrolytic lesions of the dorsal rostral pons prevent adrenocorticotropin increases after hemorrhage.

To determine if a discrete area of the dorsal rostral pons in the region of the locus coeruleus (LC) is essential for the reflex response of ACTH to hemorrhage, chloralose-anesthetized cats with bilateral electrolytic (11 cats) or sham (3 cats) lesions were challenged with a 15 ml/kg X 3 min hemorrhage. Sequential arterial blood samples taken at -6, -3, 3, 6, 9, 15, and 21 min from hemorrhage were analyzed for ACTH content. Cats were grouped according to whether plasma ACTH increased in response to hemorrhage. Bilateral lesions in 7 cats with an area in common, which lay within the LC complex, blocked the reflex increase in plasma ACTH in response to hemorrhage which was seen in 3 sham-lesioned cats, in 3 cats with lesions that did not infringe in this region bilaterally, and in 1 cat with lesions that infringed only on the medial-ventral aspect of the LC-subcoeruleus. These findings suggest that hemodynamic information responsible for the reflex response of ACTH to hemorrhage of this magnitude passes through a discrete region of the dorsal rostral pons.

Adrenocorticotropic Hormone↗
PubMed1983

Control of water intake: evidence for the role of a hemodynamic pontine pathway.

Hypovolemia increases water intake. Bilateral lesions of a discrete region of the dorsal rostral pons, that contains neurons responding to hypovolemia, markedly increases basal water intake in cats. The critical region appears anteroventral and somewhat medial to the locus coeruleus and is anatomically distinct from a more dorsal region shown previously as essential for compensation of arterial pressure in response to hypovolemia.

Adrenocorticotropic Hormone↗
PubMed1981

Right atrium mediates a vasomotor reflex.

To examine the role of right atrial receptors in mediating reflex vascular responses we measured, in cats anesthetized with chloralose/urethan, changes in mean arterial pressure (MAP) in response to volume pulsation of the right atrium (+/- 1 ml, 1 Hz). Changes in MAP were measured 1) with pressure in the carotid arteries normal and vagus nerves intact: right atrial pulsation led to a very small and transient fall in MAP; 2) with pressure in the carotid arteries at 75 mmHg and the vagus nerves intact: right atrial pulsation led to a larger and sustained fall in MAP; 3) with pressure in the carotid arteries at 75 mmHg and the vagus nerves cooled or sectioned bilaterally: right atrial pulsation of the right atrium led only to a very small and transient fall in MAP. These data suggest strongly that signals from right atrial receptors traveling in the vagus nerves mediate a reflex change in MAP that is normally masked by signals from carotid receptors.

Animals↗
PubMed1980

Metabolic profiles of penaied shrimp: dietary lipids and ovarian maturation.

The major impediment to the culture of penaeid shrimp in captivity in the United States has been an inability to obtain ovarian maturation and spawning. Lipid profiles of tissues (gonads, hepatopancreas, and tail muscle) of Penaeus setiferus caught at sea have shown that cholesterol is the dominant sterol and that polyunsaturated fatty acids known to be essential in man comprise a significant portion of the fatty acid fraction. A prioprietary marine ration contains cholesterol, but is devoid of polyunsaturated fatty acids. Ovarian maturation and spawning were obtained when the shrimp diet was supplemented with an annelid rich in lipids containing these compounds. The biochemical significance of these findings is discussed.

Animal Nutritional Physiological Phenomena↗
PubMed1980

Neurons in the dorsal rostral pons process information about changes in venous return and in arterial pressure.

To examine pathways in the brain stem that process information from cardiovascular receptors we tested, in cats anesthetized with chloralose/urethane, 76 neurons in the locus coeruleus and locus subcoeruleus for their response to hemodynamic perturbations. The experiments were designed to define processing of information from arterial baroreceptors and from atrial receptors. We have modified the activity of baroreceptors and/or atrial receptors using partial constriction of the supradiaphragmatic inferior vena cava, with and without stabilization of arterial pressure and have modified the activity of atrial receptors directly using volume pulsation of the right atrium (+/- ml, 1 Hz, 3 min). The activity of 26 neurons increased and the activity of two neurons decreased in response to constriction of the vena cava. A quantitative analysis indicates that the behavior of these neurons is related in part to changes in arterial pressure and in part to changes in other pressures, such as atrial pressure. None of the neurons stimulated by constriction of the vena cava responded to volume pulsation of the right atrium. However, 6 of 9 responsive neurons tested responded also to contriction of the vena cava during stabilization of arterial pressure. Under this condition the neurons must be responding to changes in the activity of cardiovascular receptors other than arterial baroreceptors. The results suggest strongly that neurons in the locus coeruleus and locus subcoeruleus process information about changes in venous return and in arterial pressure. It is hypothesized that the responsive neurons may mediate changes in the release of pituitary hormones and in behavioral arousal in response to hemodynamic change.

Animals↗
PubMed1978

Parabrachial pons mediates hypothalamically induced renal vasoconstriction.

The role of the parabrachial region of the dorsal rostral pons (PB) in mediating control of renal blood flow and of systemic arterial blood pressure was investigated in nine cats anesthetized with chloralose-urethan. Electrical stimulation through electrodes placed stereotaxically in lateral and medial positions in the hypothalamus (LH and MH) in PB and in ventrolateral reticular formation (VLRF) of each cat elicited pronounced systemic arterial pressor responses and renal vasoconstrictions. Stimulation parameters were adjusted so that renal flow responses elicited from each site were equal. Following a unilateral lesion in the PB, responses of renal vasoconstriction induced by hypothalamic stimulation were attenuated, but responses of arterial pressure were not altered. Stimulation of the VLRF, posterior to the lesion, consistently produced undiminished systemic pressor responses and renal vasoconstriction throughout the durations of the experiments excluding decay of renal vascular responsiveness. Thus, the data suggest that pathways mediating renal vasoconstriction in response to hypothalamic stimulation was discrete and pass through the parabrachial region, whereas pathways mediating systemic vasoconstriction in response to hypothalamic stimulation are distinct or less compact.

Animals↗
PubMed1978

Inhibitory and facilitatory areas of the ventral midbrain mediating release of corticotropin in the cat.

To examine the role of the ventral midbrain in the control of release of ACTH, we stimulated electrically 92 sites in the mesencephalon of 15 cats anesthetized with chloralose/urethane. Responses of arterial pressure could not account for change of release of ACTH. Three active areas were identified. First, in a dorsal facilitatory area that includes the dorsal longitudinal fasciculus, electrical stimulation led to changes in ACTH of +106, +117, and +90 pg/ml at 1.5, 3.5, and 6.5 min, respectively (P less than 0.05). Second, in a more ventral inhibitory area that includes the mammillary peduncle, electrical stimulation led to changes in ACTH of -63, -72, and -47 pg/ml, respectively (P less than 0.05). Third, in a ventral facilitatory area that includes the ventral tegmental area of Tsai, electrical stimulation led to changes in ACTH of +57, +56, and +59 pg/ml, respectively (P less than 0.01). The inhibitory and facilitatory areas of the ventral midbrain appeared to be continuous, respectively, with the inhibitory and facilitatory areas mediating control of ACTH in the dorsal rostral pons and in the hypothalamus. Anatomical evidence indicates projections from these ACTH-active areas of the midbrain and of the pons to ACTH-active areas of the hypothalamus. Thus, the present results suggest that the midbrain areas identified may represent pathways from ACTH-active areas of the pons to the hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1978

Organization of the medial hypothalamus for control of adrenocorticotropin in the cat.

To examine the role and interrelations of areas of the medial hypothalamus in the control of release of ACTH, we stimulated electrically (20-sec train, 200-microamperemeter amplitude at 100 Hz) 695 sites in the hypothalamus of 91 cats anesthetized with chloralose-urethane. Changes in ACTH were measured by RIA. Responses of arterial pressure could not account for changes of release of ACTH. Several ACTH-active areas were defined. The anatomical relations of these areas with known nuclei and pathways then were considered. Two ACTH facilitatory areas and one ACTH inhibitory area were identified in the lateral aspect of the medial hypothalamus. The dorsal facilitatory area appears to be an extension of the lateral division of the dorsolongitudinal fasciculus and to extend medially to join the Fields of Forel, the ventral tegmental area of Tsai, and the parvocellular, paraventricular, and periventricular nuclei. The ACTH inhibitory area appears to be an extension of portions of the central tegmental tract and to extend medially to the posterior hypothalamic area and the dorsal hypothalamic area and ventrally toward the basal hypothalamus. The ventral ACTH facilitatory area appears to be coincident with the medial forebrain bundle and to extend anteroventrally and medially through the supraoptic decussation to the suprachiasmatic, ventromedial, dorsomedial, periventricular, infundibular, and premammillary nuclei. Stimulation of the median eminence led to increased release of ACTH. The results suggest that ascending pathways from the lower brainstem mediating control of ACTH project to discrete areas of the hypothalamus and then converge on the medial basal hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1977

Neural control of ACTH release in response to hemorrhage.

A three dimensional reconstruction of the central neural pathways that appear to mediate release of ACTH in response to hemodynamic change is illustrated in Figure 11. Fibers from receptors in the right atrium and the carotid arteries project to the lateral solitary nucleus and then to the medial and the lateral nucleus intercalatus. A pathway containing projections from these nuclei then converges dominantly in the locus subcoeruleus and locus coeruleus. Multiple pathways then diverge, to travel in part directly to the hypothalamus through dorsal pathways. One pathway inhibits and another facilitates the release of ACTH. Multiple pathways also diverge, to travel in part medially, and then to the hypothalamus through ventral pathways. Again, one pathway inhibits and another facilitates the release of ACTH. The dorsal and ventral inhibitory pathways appear to converge in a region extending from just caudal and ventral to the paraventicular nucleus to the posterior hypothalamic area. Thus, after the coalescences of the various pontine-hypothalamic pathways, three principal pathways remain. These include a posterior inhibitor path, an anterodorsal facilitatory path that terminates in the paraventricular nucleus and that may be mediated through release of vasopressin, and an anteroventral facilitatory path that terminates in the suprachiasmatic and ventromedial nuclei and that is probably mediated through release of corticotropin-releasing hormone. The mode of integration of these pathways has not been defined. The pathways described herein are oligosynaptic: a signal may travel from atrium to hypothalamus over three to seven neurons. The combination of control of input hemodynamic signals and of measurement of ACTH permits quantitation of both sensory and motor events, that inevitably must be embedded in the neuronal pathways described here. The analysis of the input-output relations and their correlation with internal neural events must form the basis of a description of the physiology of the physiology of the system whose central neural anatomy has been defined in part by these studies.

Adrenocorticotropic Hormone↗
PubMed1977

Neurons in medullary areas controlling ACTH: atrial input and rostral projections.

To examine hindbrain pathways mediating release of adrenocorticotropin (ACTH) in response to hemodynamic changes we tested, in 19 cats (chloralose/urethan), 70 neurons in ACTH-active areas of the medulla for their response to volume pulsation (+/- 1 ml, 1 Hz, 60 s) of the right atrium (RA) or to hemorrhage (3 ml/kg per 30 s), and to electrical stimulation in ACTH-active areas of the dorsal rostral pons (DRP). The activity of 16 neurons was increased (P less than 0.05) by RA. Of these, 6 were driven antidromically from the locus subcoeruleus (LSC), and were located in the lateral solitary nucleus and in posteromedial nucleus intercalatus (NI). The activity of 11 neurons was decreased by RA. Of these, 5 were driven antidromically from LSC and lateral ventral tegmental nucleus and were located in anterolateral NI. No rostral projections were found to more medial sites in DRP. Responses to the first trial of RA were rapid, but slowed and attenuated with repeated trials. Responses to hemorrhage were rapid and in the opposite direction, but did not attenuate. The results suggest that pathways displaying rate sensitivity project from the right atrium via B-receptors to the DRP.

Adrenocorticotropic Hormone↗